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How Dementia Affects The Brain

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How Dementia Affects The Brain

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Sleep Deprivation Increases Alzheimer’s Protein

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Remi L. Landry by Remi L. Landry Scilit Preprints.org

Department of Tropical Medicine, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA 70112, USA

Study Finds That Exercise Results In Larger Brain Size And Lowered Dementia Risk

Received: 13 April 2022 / Revised: 7 May 2022 / Accepted: 11 May 2022 / Published: 17 May 2022

The potential contribution of pathogenic microbes to disease causing dementia is a matter of considerable importance. Alzheimer’s disease (AD) is a neurocognitive disease that slowly destroys brain function, leading to cognitive impairment and behavioral and psychiatric disturbances. The histopathology of AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by accumulation of amyloid-β (Aβ) peptide in the form of parenchymal plaques and abnormally aggregated tau protein in the form of neurofibrillary tangles. Observational, epidemiological, experimental and pathological studies have generated evidence for the complexity and possible polymicrobial causal relationships in diseases causing dementia. The AD pathogenesis hypothesis states that pathogens and microbes act as triggers, interacting with genetic factors to initiate the accumulation of Aβ, hyperphosphorylated tau protein (p-tau), and inflammation in the brain. Evidence suggests that Borrelia sp., HSV-1, VZV (HHV-2), HHV-6/7, oral pathogens, Chlamydophila pneumoniae and Candida albicans can infect the central nervous system (CNS), evade the immune system and consequently prevail. AD brain. Researchers have made significant progress in understanding the multifactorial and overlapping factors believed to be involved in the etiopathogenesis of dementia; However, the cause of AD remains unclear.

Neurodegenerative diseases are receiving increasing attention because they represent a major public health problem with significant socioeconomic impact, affecting more than 50 million Americans each year. As the population of aging Americans grows rapidly and lives longer due to advances in social and environmental conditions, the number of people living with neurodegenerative disorders will increase. Neurodegenerative disorders are defined as rare, age-related, and genetic conditions characterized by cognitive impairment [ 1 ]. Many factors are associated with neurodegenerative disease, including genetics, nutritional deficiencies, environmental factors, infectious agents, and certain metals [2]. These factors and others can cause changes in brain biochemistry and nerve cell signaling, leading to neuronal degeneration, cell dysfunction, and nerve death, leading to neurological disorders and dementia. The most problematic neurodegenerative diseases are Alzheimer’s disease (AD), Lewy body dementia, amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD), multiple sclerosis (MS), prion diseases and other dementias. The clinical manifestations of a particular neurodegenerative disease reflect the type of pathological protein that accumulates, the brain regions affected, and the types of neurons that undergo cytotoxic events (Figure 1). Although neurodegenerative disorders have traditionally been clinicopathologically distinct entities, it is increasingly recognized that the clinical presentations of the disorders may overlap. Significant clinical and neuropathological overlap of two or more disorders is not uncommon. For example, patients with frontotemporal dementia (FTD) may have ALS, patients with FTD may develop symptoms similar to PD, and many patients with Lewy body dementia have overlapping AD [ 3 ]. AD pathology is described by Braak staging, as multiple regions are sequentially involved (Figure 1 [4]).

Dementia is a serious health problem in the industrialized world [5]. A large group of the American population – the baby boom generation – is beginning to reach the age of 65 and older, the age range when the risk of Alzheimer’s and related dementias is highest [6]. In 2021, the population of Americans aged 65 and older was estimated at 58 million, but this number is expected to grow to 88 million by 2050 [7]. Consequently, the prevalence of AD among those aged 65 and older is expected to increase from the current estimate of 6.2 million people to 13.8 million by 2060 [5]. AD is officially listed as the sixth leading cause of death in the United States and the fifth leading cause of death for those aged 65 years and older [ 8 ].

Stroke, Brain Injury, And Dementia: Is There A Link?

Alzheimer’s disease and related dementias are caused by a chronic inflammatory neurodegenerative disease process that slowly destroys brain function, leading to cognitive impairment, behavioral and psychiatric disturbances, and decline in activities of daily living. Most often, AD manifests as progressive amnesia-predominant multidomain cognitive impairment [9]. Often, a gradually declining memory is an early cognitive deficit. In most cases, the ability to communicate and perform activities of daily living is greatly impaired [10]. Other deficits such as behavioral disturbances, personality changes, visual disturbances, and motor and sensory deficits manifest in advanced stages or atypical presentations of the disease [ 11 , 12 , 13 , 14 ]. Atypical presentations, including posterior cortical atrophy (PCA), primary progressive aphasia (PPA) and frontal variant AD, pose a diagnostic challenge to researchers and clinicians [ 9 , 15 ]. These atypical forms of AD account for 5% of AD patients over 65 years of age and approximately one-third of AD patients under 65 years of age [ 14 , 16 ]. The aim of this review is to assess the evidence for the role of microbes and possible mechanisms of pathogenesis in the development of Alzheimer’s and related dementias.

For now, a primary diagnosis of AD is largely ruled out. Clinical history, psychiatric and neurological examination, cognitive testing, and neuroimaging can all help rule out other common neurodegenerative disorders. In the last 20 years, AD Cerebrospinal fluid (CSF) biomarkers, total tau (T-tau), phosphorylated tau (p-tau) and amyloid-β (Aβ 42), have shown consistently high diagnostic accuracy for AD dementia [17]. Positron emission tomography (PET) imaging with amyloid-beta (Aβ) tracers and 2-[18F] fluoro-2-deoxy-d-glucose (FDG) is a promising tool for the early detection of AD [ 18 ]. FDG-PET for AD pathology is a first-class method for detecting brain changes in vivo in preclinical and early AD [ 18 ]. For a definitive diagnosis, which is considered the gold standard, clinical evaluation of possible AD is required after biopsy or histopathological examination of postmortem brain tissue for the presence of neurofibrillary tangles and amyloid plaques. The diagnosis of AD is further complicated by the similar clinical symptoms of other neurodegenerative diseases.

Alzheimer’s disease is classified into two distinct forms: early-onset AD (EOAD) or sporadic late-onset AD (LOAD) [19]. Progress has been made in understanding the underlying pathological components in the AD brain, both for early-onset and late-onset forms [20]. Both EOAD and LOAD share common characteristics, including oxidative stress, up-regulated inflammatory signaling, accumulation of lesions and plaques, synaptic signaling deficits, atrophy, altered gene expression, and cognitive impairment.

Lewy body dementia includes dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB and PDD are clinically similar diseases in that they share characteristic neuropathological changes, including α-synuclein accumulation in Lewy bodies and loss of tegmental dopamine cell populations and cholinergic basal forebrain populations; These often coexist with AD pathology [21]. Clinical manifestations of DLB ​​and PDD include progressive cognitive impairment associated with parkinsonism, visual hallucinations, delusions, and fluctuations in attention and alertness [22]. While AD affects the brain’s ability to store new information in the form of memories, DLB targets different cognitive functions, including problem solving and reasoning. In general, women have a higher chance of developing AD, while men have a higher risk of DLB. Patients with DLB and PDD often have difficulty walking and struggle with balance, but physical deterioration does not usually occur in AD. Clinical differentiation between DLB and PDD is based on differences in the time of onset of parkinsonism and cognitive symptoms [22].

Certain Personality Traits May Affect Risk Of ‘pre Dementia’

Early onset, usually before the age of 65 years, is a rare familial form of AD, accounting for approximately <5% of all cases of the disease [23]. Current estimates do not include people with Down syndrome (DS), but EOAD should

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